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. 1998 Jan;27(1):158-66.
doi: 10.1016/s0741-5214(98)70303-9.

Monocyte Infiltration Into Venous Valves

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Monocyte Infiltration Into Venous Valves

T Ono et al. J Vasc Surg. .

Abstract

Purpose: Greater saphenous veins removed at surgery for correction of venous dysfunction have few valves. Those that are present may be shrunken, deformed, or monocuspid. This study was carried out to determine whether leukocyte infiltration is associated with valve damage.

Methods: Seventeen specimens were removed at surgery from five men and eight women (age, 29 to 80 years). These consisted of the proximal 15 cm of the duplex-confirmed, refluxing proximal greater saphenous vein, one proximal lesser saphenous vein, and one midportion of greater saphenous vein. The severity of venous stasis in each patient limb was classified by the CEAP formula. Twelve were class 2, two were class 3, and three were class 4. Control specimens were obtained from patients who underwent coronary artery bypass grafting. These were two men and two women, ages 72, 66, 62, and 60 years, free of venous insufficiency, with the specimens obtained from the proximal saphenous vein. Two of the control specimens contained venous valves corresponding to the test specimens. Longitudinal 10 microns paraffin sections were labeled with anti-CD64 monoclonal antibody, specific for tissue monocytes and macrophages, and studied by light microscopy. Five regions were chosen for quantification of the leukocyte infiltrate. Cells were categorized and counted directly. Volume proportions were calculated using stereologic techniques.

Results: Three of seven specimens studied for morphologic changes had clearly shortened valve leaflets. Collagen degeneration was noted in all seven specimens. Leaflets had essentially disappeared in three and were shortened to 100 to 2100 microns in five. Specific leukocyte staining was accomplished on 10 additional specimens. All specimens showed monocyte/macrophage infiltration in valve leaflets and venous wall. These were more numerous in the valve sinus and proximal wall both on and under the endothelium. Control specimens showed no monocyte/macrophage infiltration.

Conclusions: These observations suggest that venous valve damage in refluxing saphenous veins is associated with a leukocyte (monocyte/macrophage) infiltrate. Cell activation and fluid dynamic factors, such as eddies recirculation, and stasis in the valve sinus may be a part of the process of leukocyte penetration of the endothelium. The magnitude of leukocyte infiltration in the vein wall and in the base of the valve leaflet may be important in the genesis of primary venous dysfunction.

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